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机构地区:[1]山东医科大学病理生理学教研室,济南250012 [2]西安病理生理学教研室,西安710061
出 处:《西安医科大学学报》1997年第3期326-328,345,共4页Journal of Xi'an Medical University(Chinese)
基 金:国家自然科学基金!39270315;"八五"攻关项目!(85-195-03-02)
摘 要:通过分离、培养心肌梗塞后成年大鼠的心肌细胞(MC),观察了血管紧张素Ⅱ(AngⅡ)在不同处理因素对照下,对MC核酸、蛋白质合成的影响。结果显示:在相同浓度的AngⅡ(10-7M)作用下,MI组MC的RNA和蛋白质的合成速率均显著高于假手术组(P<0.05)。AngⅡ的上述作用,可分别被AT1受体阻滞剂Losartan、特异性AngⅡ拮抗剂[1,3]AngⅡ和血管紧张素抗肽(Amg-AP)完全阻断。结果提示:AngⅡ可直接作用于非梗塞区心肌的MC,促进MC的RNA、蛋白质合成;介导AngⅡ对MC的作用是AT1受体。In the present study, the method of isotope-lablled substrate incorporation was used to investigate the effect of angiotensin Ⅱ on the synthe-ses of RNA and protein of isolated myocardial cells (MC) from rats in different conditions. The results showed that the rates of 14C-UR and 3H-Leu in-coporating in MC were significantly higher in my-ocardial infarction(MI) group than in sham-operated (SO) group, respectively. Theses effects of ang Ⅱon MCs were abolished completely by using either angiotensin receptor antagonits, Losatan, or an-giotensin anologue, 1.8Ang Ⅱ, or angiotensin an-tipeptide. Meanwhile, the mean protein cotent in a single MC was markedly higher in MI group than in SO group, too. The findings suggest that Ang Ⅱ can improve the syntheses of RNA and protein in non-infarcted myocytes, and AT1 receptor is the me-diator which transducts anR Ⅱ siRnal into MC.
分 类 号:R542.22[医药卫生—心血管疾病]
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